An antibody-drug conjugate (ADC) targeting B7-H4 (VTCN1) on tumor cells; after binding, it is internalized and releases a cytotoxic payload to kill B7-H4-expressing cancer cells.
Monoclonal antibody targets B7-H4 (VTCN1) on tumor cells; upon binding and internalization, it releases an attached cytotoxic payload inside the cell, leading to apoptosis of B7-H4–expressing cancer cells.
YES
DIRECT
The ADC binds B7-H4 on target cells, is internalized, and releases a cytotoxic payload intracellularly, inducing apoptosis of B7-H4–expressing cells.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy redirecting cytotoxic T cells to CD19-expressing B cells.
Autologous T cells engineered with an anti‑CD19 chimeric antigen receptor containing CD28 costimulatory and CD3ζ signaling domains; upon infusion, CAR T cells bind CD19 on B cells, become activated, proliferate, release cytokines, and mediate cytotoxic killing of CD19‑expressing malignant B cells.
YES
DIRECT
Anti-CD19 CAR-T cells bind CD19 on B cells and, upon activation via CD28/CD3ζ, induce cytolytic killing through perforin/granzyme-mediated apoptosis and cytokine release.
Autologous anti-CD19 CAR T-cell therapy that targets CD19 on malignant B cells to mediate T-cell cytotoxicity.
Autologous T cells engineered to express an anti‑CD19 chimeric antigen receptor with a 4‑1BB (CD137) costimulatory domain and CD3‑zeta signaling. Upon binding CD19 on malignant B cells, the CAR triggers T‑cell activation, proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of CD19‑positive tumor cells.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 and, upon activation, kill CD19+ cells via perforin/granzyme-mediated cytolysis (and death receptor signaling).
Autologous anti-CD19 CAR T-cell therapy composed of defined CD4+ and CD8+ T-cell subsets engineered to target CD19.
Autologous CD4+ and CD8+ T cells engineered with an anti-CD19 chimeric antigen receptor (scFv-4-1BB-CD3zeta). Upon binding CD19 on B-cell malignancies, the CAR triggers T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD19+ cells. The 4-1BB domain enhances persistence and antitumor activity, and a truncated EGFR allows tracking and potential elimination with cetuximab.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 and directly kill CD19+ cells via T-cell cytotoxic mechanisms (perforin/granzyme-mediated lysis and death-receptor pathways).
Anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 and eliminates CD20+ cells via complement-dependent cytotoxicity and Fc-mediated ADCC (NK cells/macrophages), and can also trigger apoptosis upon CD20 crosslinking.